BURNS

A burn is a injury which is caused by application of heat or chemical substance

to the external or internal surfaces of the body, which causes destruction of the
tissues.

Epidemiology :

. morethan 90% of burns are caused by carelessness or ignorance and are

completely preventable; nearly half are smoking or alcohol related.

. burn deaths generally occur in bimodal distribution, either immediately after

the injury or weeks later as result of multi-organ failure.

. 2/3 of all burns occur at home and commonly involve young adult men,
children <15yrs & the elderly.

. 75% of all burns related deaths occur in house fires.

. young adults are frequently burned with flammable liquids, and toddlers are
often scalded by hot liquids...

Etiology :
1. Thermal : a) Heat
b) Cold
2. Chemicals

3. Electrical
4. Radiation

1) Thermal burns
a) Heat: when heat is applied to skin, the depth of injury is proportionate
to the temperature applied, the duration of contact & the thickness of
skin.
i) Scald burns: Most common form of burns. It results from
application of liquid >60 degree Celsius or from steam.

Degree of scalds: a) erythema by vasoparalysis

b)blister formation due to increased
capillary permeability.
c)necrosis of the dermis.

Exposed areas tend to be burned less deeply than areas

covered with thin clothing as clothing retains heat &
keeps the liquid in contact with the skin for a longer time

ii) Flame burns: Next most common. Due to improper usage

flammable liquids, automobile accidents & ignition of
clothing from stove.

iii) Flash burns: Next in frequency, explosions from natural

gas, propane, gasoline cause intense heat for a very brief
time.

Flash burns are mostly dermal, their depth depending

amount & kind of fuel that explodes.

iv) Contact burns: Results from contact with hot metals

plastic, glass or hot coal; usually limited in extent but
invariably very deep. Contact burns are often fourth
degree burns.

b) Cold: Caused by exposure to cold which include freezing & non

freezing injuries.
i) Non freezing injuries: Occur due to prolonged exposure to
severe cold & dampness, usually extremities are affected. Eg
:trench foot, immersion foot
 ii) Freezing injuries: Occurs due to extremes of cold which
develops rapidly & in addition to extremities, it frequently
affects other parts like nose, ears, the face.

Frost bite mostly affects the skin and subcutaneous tissues, tissue
necrosis following frostbite is related primarily to the mechanical effects of ice
crystals, cellular dehydration & microvascular occlusion.
Degrees: a) 1st degree : hyperaemia & edema without necrosis.
b)2nd degree: hyperaemia, vesicle formation & partial necrosis
of the skin.
c) 3rd degree: necrosis of full thickness skin including
subcutaneous tissue & all underlying structures including muscle &
bone. This leads to gangrene of the affected part.

2) CHEMICAL BURNS
Most chemical burns are accidental. The degree of tissue damage is
determined by the chemical nature of the agent, the concentration of the
agent and the duration of skin contact. Chemicals cause their injury by
protein destruction, with denaturation, oxidation and formation of protein
esters.
a) ALKALI BURNS: Alkali’s such as lime, potassium hydroxide and
sodium hydroxide are the most common agents involved in chemical
injury... 3 factors are involved in mechanism of alkali burns..
i) Saponification of fat causes loss of insulation of heat formed in
chemical rxn with tissue.
ii) Massive extraction of water from cells causes damage because
of the hygroscopic nature of the alkali’s.
iii) Alkali’s dissolve & unite with proteins of tissues to form
alkaline proteinates, which are soluble & contain hydroxide ions

b) ACID BURNS: Acids induce protein breakdown by hydrolysis which

results in hard eschar that does not penetrate as deeply as alkalis do.
These agents also induce thermal injury by generation of heat after
contact with skin, thus causing additional soft tissue damage.
 3) Electrical burns:
These are caused by high-voltage electric current. It causes
minimal damage to the skin. The skin is involved at 2 points- at the point of
contact with the electrical source & at the site of exit at which the patient is
grounded. The magnitude of the injury is related to:
a) Type of current: AC is 5 times dangerous as equal voltage of DC.
b) Amount of current: electrocution is rare at < 100volts,& most deaths
occur at > 2000volts.
c) Path of current: death is more likely to occur if the brain stem is
involved.
d) Duration of current flow: severity is directly proportional to duration
of current flow.
Electrical burns are usually divided into low voltage and high voltage injuries,
the threshold being 1000volts.
a) Low voltage injuries: these do not have enough energy to cause
destruction to significant amnt of subcutaneous tissues when the current
passes through the body. The resistance is too great. The entry and the exit
points, normally in the fingers and toes suffer small deep burns. These
may cause underlying tendon and nerve damage. The AC creates a tetany
within the muscles. The main danger is that the AC interferes with normal
cardiac pacing which may cause sudden cardiac arrest.
b) High voltage injuries: can be caused by one of the following 3 sources of
damage: the flash, the flame, the current itself.

4) RADIATION BURNS: It is usually caused by X-rays or radium. This only

occurs when the tissue has been irradiated beyond its tolerance level. 2
types of radiodermatitis are usually seen:
.Acute radiodermatitis: presents with usual changes of acute inflammation with
erythema, varying degrees of edema & exfoliation.these develop on or about the
5th day.
.Chronic radiodermatitis: may occur if small doses of irradiation are given for
too long time. Skin shows irregular pigmentation or depigmentation in certain
areas, telegectasias & small indolent ulcers.
PATHOPHYSIOLGY OF BURNS
LOCAL CHANGES

Burns causes coagulative necrosis of the epidermis & underlying tissues, with
the depth depending on the temperature to which the skin is exposed & the
duration of exposure. The specific heat of the causative agent also affects the
depth.
The skin provides a robust barrier to transfer of energy to deeper tissues,
therefore much of the energy is confined to this layer. After the inciting focus is
removed, the response of local tissues can lead to injury to deeper layers. The
areas of cutaneous injury can be divided in to 3 zones:
1. Zone of coagulation: the necrotic area of burn where cells have been
disrupted, this site is irreversibly damaged at the time of injury.
2. Zone of stasis: area immediately surrounding the necrotic zone. Has a
moderate degree of insult with reduced tissue perfusion. Depending upon
wound environment, it can either survive or progress to coagulative
necrosis. This zone is associated with vascular damage and vessel
leakage.
3. Zone of hyperaemia: characterized by vasodilatation fro inflammation of
surrounding the burn wound. This region contains clearly viable tissue
from which healing process begins & is generally not a risk for further
necrosis.
Burn depth
The depth of a burn depends upon the degree of tissue damage. Burn depth is
classified according to the degree of injury in epidermis, dermis, subcutaneous
fat, & underlying structures.
1. 1st degree burns: Confined to the epidermis. These burns are painful &
erythematous, blanch to the touch & have intact epithelial barrier. These
do not result in scarring & trt is aimed at comfort with use of topical
soothing salves & oral NSAID’s.
2. 2nd degree burns: Divided into 2 types- Superficial & Deep.
All 2nd degree burns have some degree of dermal damage, & the destruction is
based on the depth of injury to this structure.
Superficial dermal burns are erythematous & painful, blanch to touch, & often
blister. These wounds spontaneously re-epithelialize from retained epidermal
structures in 7-14days. It may result in some slight discoloration over long term.
Deep dermal burns extend into reticular layer of the dermis, appear more pale &
mottled, do not blanch to touch, but remain painful to pin-prick. These heal in
14-35days by re-epithelialization from hair follicles & keratinocytes often with
severe scarring as result of loss of dermis.
3. 3rd degree burns: Are full thickness through the epidermis, dermis, & are
characterized by hard, leathery eschar that is painless & black, white or
cherry red. No epidermal or dermal appendages remain, thus these
wounds must heal by re-epithelialization from wound edges.
4. 4thdegree burns: Involve other organs beneath the skin, such as muscle,
bone.
Burn size
.Determination of burn size estimates the extent of injury, burn size is usually
assessed by “ Rule of nine “.
.Another method of estimating smaller burns is to consider the area of the open
hand to be approx 1% of TBSA & then transpose that measurement visually
onto the wound for determination of the size, this method is helpful when
evaluating splash burns & other burns of mixed distribution.
.Lund and Browner method.

SYSTEMIC CHANGES

1) Inflammation and edema

Significant burns are associated with massive release of
inflammatory mediators, both in and around other tissues. These mediators
produce vasoconstriction, vasodilatation, increased capillary permeability, and
edema locally & in distant organs.
Initially interstitial hydrostatic pressure decreases dramatically in the burned
skin, & there is associated slight increase in interstitial pressure in non-burnt
skin.
Increased capillary permeability
 Protein loss

Plasma oncotic pressure decreases and interstitial oncotic pressure increases

Edema forms in the burned & non – burned skin

The edema is now more in burned tissue because of lower interstitial pressure.

Mediators which lead to increased permeability: Histamine , bradykinin,

vasoactive amines, prostaglandins, leukotreines, activated complements,
catecholamines. Aggregated platelets release serotonin, which plays major role
in edema formation. Serotonin directly acts to increase pulmonary vascular
resistance and it directly aggrevates the vasoconstrictive effects of various
vasoactive amines. Thrombaxene A2 plays a major role in changes in
permeability and fluid shifts. It leads to vasoconstriction & platelet aggregation
in the wound, thereby contributing to zone of stasis.

Microvascular changes include cardiopulmonary alterations characterized by:

a) Loss of plasma volume.
b) Increases peripheral vascular resistance.
c) Decreased cardiac output due to reduced blood vol, increased blood
viscosity, reduced cardiac contractility.

2) Effects on the renal system:

Diminished blood vol reduced cardiac output reduced renal blood flow
reduced GFR oliguria acute tubular necrosis and renal failure.

Other sress-induced hormones & mediators which reduce RBF immediately

after injury- angiotensin, aldosterone, vasopressin.
Early resuscitation decreases renal failure & improves mortality rate.
 3) Effects on GI system:
GI response to a burn is evidenced by mucosal atropy, changes in digestive
absorption & increased intestinal permeability.
Atrophy of the small bowel mucosa occurs within 12hrs of injury in proportion
to the burn size & is related to increased epithelial cell death by apoptosis.
Burns also causes reduced uptake of glucose and amino acids, decreased
absorption of fatty acids & reduction in intestinal brush border lipase activity.
These changes peak in the first several hours after a burn & return to normal at
48-72hrs after the injury.
Intestinal permeability to macromolecules increases after a burn, gut
permeability increases further when burn wound becomes infected.

4) Effects on the Immune system:

Burns cause global depression in immune function. Burns patients are at greater
risk for a number of infectious complications, including bacterial wound
infection, pneumonia & fungal & viral infections. These susceptibilities &
conditions are based on depressed cellular function in all parts of the immune
system, including activation of neutrophils, macrophages, T lymphocytes and B
lymphocytes.

.Macrophage production after burn is decreased due to the spontaneous

elaboration of negative feedback regulators of myeloid growth.
.Total neutrophil counts are initially increased after a burn, which is related to a
decrease in cell death by apoptosis. The neutrophils that are present are
dysfunctional in terms of diapedesis, chemotaxsis & phagocytosis. After 72hrs,
neutrophils count is decreased.
.Burns also impair cytotoxic T-lymphocyte activity, thus increasing the risk for
infection particularly for fungi and viruses.

5) Hypermetabolism :
Characterized by tachycardia, increased cardiac output, elevated energy
expenditure, increased oxygen consumption, proteolysis & lipolysis, & sever
nitrogen loss, develops after sever burns and resuscitation. May be sustained for
months and lead to weight loss and decreased strength. These alterations are due
to release of catabolic hormones which include catecholamines, glucocorticoids
& glucagon.
.Catecholamines act directly & indirectly to increase glucose availability
through hepatic gluconeogenesis & glycogenolysis.
.Glucocorticoidshormones released by the way of H-P-A are mediated through
neural stimulation. It increases insulin resistance which is addictive to
hyperglycemia.
.Peripheral lipolysis, mediated through the catabolic hormones is also a
priniciple component metabolic response to severe burn.

Elevation of catabolic hormones------------------- stimulation of hormone

sensitive lipases in adipocytes--------------release of FFA---------- oxidized for
energy & re-esterified to TG-------------- further packed for transport to other
tissues by way of VLDL----------deposited in liver.
. Glycerol from breakdown of fats enters the gluconeogenic pathway. The
development of fatty liver in this situation is thought to be secondary to the
overloading of normal processing enzymes or down regulation of fatty acid
handling mechanisms.

6) Burn Shock:
. Burn shock is a complex process of circulatory & microcirculatory
dysfunction, not easily or fully repaired solely by fluids.
. Burn shock is hypovolemic & cellular in nature & is characterized by specific
hemodynamic changes including reduced cardiac output, ECF, plasma vol &
oliguria.
. One major component of burn shock is the increase in total body capillary
permeability. Direct thermal injury results in marked changes in the
microcirculation most of which occurs locally at the burn site.
.Thermal injury also causes changes at cellular level. In burns >30% TBSA,
there is systemic decrease in cell transmembrane potential involving non-
thermally injured cells which results from an increase in intracellular sodium
concentration secondary to decrease in sodium ATPase activity responsible for
maintaining the IC-EC ionic gradient...

INHALATIONAL INJURY

• Major factor contributing to death in burn injury patients.

• Smoke impedes normal gas exchange vital for critically injured patients.
• With inhalational injury, damage is primarily by inhaled toxins. Heat is
dispersed in upper airways, whereas the cooled particles of smoke &
toxins are carried distally to the bronchi. The injury to the airway is
basically chemical in nature.
• Response to smoke inhalation is an immediate increase in blood folw in
the bronchial arteries to the bronchi along with edema formation &
increase in lung lymph flow.
• There is separation of ciliated epithelial cells from the basement
membrane followed by formation of exudates within the airways.
Exudates consists of proteins found in lung lymph, &it coalesces to form
fibrin casts.
• Often seen with clinical H/O exposure to smoke in a closed space,
hoarseness, wheezing. Diagnosis must be established by use of
broncoscopy.
Clinical course of patients with inhalational injury is divided into 3 stages:
1) Acute pulmonary insufficiency
2) 2nd stage occurs after 72-96hrs after injury & is associated with hypoxia
& development of diffuse lobar infilterates, clinically similar to ARDS.
3) 3rd stage, clinical broncopneumonia predominates, occurs 3-10days after
inhalational injury

MANAGEMENT
IMMEDIATE CARE
. Ensure rescuer safety
. Stop the burning process
. Check for injuries
. Cool the wound
. Give oxygen

HOSPITAL CARE

. Secure Airway
. Breathing, Ventilation
. Circulation
. Disability – neurological status
. Fluid resuscititation

MAJOR DETERMINANTS OF OUTCOME OF

BURN
.Percentage of surface area burnt
.Depth of burns
.Presence of inhalational injury

ASSESSMENT OF BURN WOUND

. Patient’s whole hand is 1% TBSA and is useful in small
burns.
.Wallace’s rule of nine can be used as a rough guide.

FLUID RESUSCITATION

.The Principle is to maintain Intravascular volume to

provide sufficient circulation to perfuse the essential
organs such as Brain, Kidney and the damaged skin.

RESUSCITATION FORMULAS

.PARKLAND FORMULA – 4 ML/KG/%TBSA

.BROOKE FORMULA – 1.5 ML/KG/%TBSA

.GALVESTON FORMULA – 500 ML/SQ M BURNED AREA +

1500 ML/SQ M TOTAL AREA.

.Ringer Lactate solution is the best choice.

.Half of the calculated fluid is given in first 8hrs from
the time of burns and the rest in next 16hrs.
.Hypertonic solution and 5% Albumin can also be used.
 MONITORING OF RESUSCITATION

.Urine output should be 0.5ml/kg/hr in adults and

1ml/kg/hr in children.
.If output is less, then the infusion rate is increased by
50%.

ESCHAROTOMY AND FASCIOTOMY

.Circumferential third degree or full thickness burns

may form an unyielding crust called Eschar.
.Eschar is incised in mid-lateral or mid-medial line.
.In a patient with chest-wall burn, it is performed in
anterior axillary line bilaterally.
.Fasciotomy is required in treatment of electrical burns
for extensive muscle injury.

WOUND CARE

.First degree wounds are minor and require no dressing,

just topical betadine solution is sufficient.
.Second degree wounds are treated with daily dressing
and topical antibiotics. Temporary biologic or synthetic
covering can be used.
.Deep second degree and third degree wounds require
excision and grafting.

ANTIMICROBIALS

.Silver Sulphadiazine is the most commonly used

topical antimicrobial and is painless on application.
.Mafenide acetate is able to penetrate eschar and
capable of suppressing dense bacterial proliferation
underneath the eschar.

WOUND MANAGEMENT

.Tangential excision sacrificies minimal living tissue and

leads to a far superior cosmetic result.
.Very thin layers os Eschar is shaved until viable tissue
is reached, it can cause massive blood loss.
.Fascial excision includes burnt tissue and
subcutaneous fat to the level of investing fascia.
.It is reserved for patients with deep burns like charred
flame burns, molten metal burns and electrical burns.
 SKIN GRAFTS AND ALTERNATIVES

Autologous split thickness can be harvested depending

upon patients age and donor site.
.Unmeshed split thickness grafts are used to cover
areas of face, hand, and burns in a child.
.Synthetic alternative to allografts is Biobrane, a sheet
of nylon mesh impregnated with collagen that is
bonded to a silicone rubber membrane.

NUTRITIONAL SUPPORT

.Burns victims develop a large catabolic process

secondary to systemic inflammatory response.

.Prevents translocation of intestinal bacteria and stress

ulcerations are prevented.

MANAGEMENT OF ELECTRICAL INJURY

.If the patient is unconscious then cardiac arrest should

be excluded and CPR is started.

.Adequate fluid replacement should be given.

.Cutaneous injury should be debrided, cleaned and
topical creams are applied.

.In case of severe injury through a limb, primary

amputation is sometimes the most effective
management.

MANAGEMENT OF CHEMICAL BURNS

.Irrigation of the affected areas with large amts of

water.
.In Phenol burns, water may accelerate its absorption,
so Polyethylene Glycol should be used.

.Tissues with frank necrosis should be excised.

.Skin grafting should be done after healthy tissue is

exposed.

MANAGEMENT OF RADIATION INJURY

.Conservative management until true extent of tissue
injury is apparent.

.If damage causes ulcer, then excision and covering

with vascularised tissue is required.

FROST BITE MANAGEMENT

Rapid re-warming followed by observation.

.Surgery is delayed until demarcation is clear.